The clinical diagnosis is confirmed following stoppage of menstruation (amenorrhea) for twelve consecutive months without any other pathology. As such, a woman declare to have attained menopause only retrospectively. Premenopausal refers to the period prior to menopause, post menopause to the period after menopause and perimenopause to the period around menopause (40–55 years), Climacteric is the period of time during which a woman passes from the reproductive to the nonreproductive stage. This phase covers 5–10 years on either side of menopause. Perimenopause is the part of the climacteric when the menstrual cycle is likely to be irregular. Post menopause is the phase of life that comes after the menopause.[1]
Age of Menopause
Age at which menopause occurs genetically predetermine. The age of menopause is not relate to age of menarche or age at last pregnancy. It is also not relate to number of pregnancies, lactation, use of oral pill, socioeconomic condition, race, height or weight. Thinner women have early menopause. However, cigarette smoking and severe malnutrition may cause early menopause. The age of menopause ranges between 45–55 years, average being 50 years.[1]
Clinical Importance
Due to increased life expectancy, especially in affluent society, about one-third of life span will be spent during the period of estrogen deprivation stage with long-term symptomatic and metabolic complications.[1]
Endocrinology of Climacteric and Menopause
Hypothalamopituitary Gonadal Axis
Few years prior to menopause, along with depletion of the ovarian follicles, the follicles become resistant to pituitary gonadotropins. As a result, effective folliculogenesis impaire with diminished estradiol production.
This decreases the negative feedback effect on hypothalamo-pituitary axis resulting in increase in FSH. The increase in FSH also due to diminish inhibin. Inhibin, a peptide, secrete by the granulosa cells of the ovarian follicle. The increase of LH occurs subsequently. Disturbed folliculogenesis during this period may result in anovulation, oligo-ovulation, premature corpus luteum or corpus luteal insufficiency. The sustained level of estrogens may even cause endometrial hyperplasia and clinical manifestation of menstrual abnormalities prior to menopause. The mean cycle length is significantly shorter. This is due to shortening of the follicular phase of the cycle. Luteal phase length remaining constant. Ultimately, no more follicles are available and even some exist, they are resistant to gonadotropins. Estradiol production drops down to the optimal level of 20 pg/mL → no endometrial growth → absence of menstruation.
Androgens:
After menopause, the stromal cells of the ovary continue to produce androgens because of increase in LH. The main androgens are androstenedione and testosterone. Though the secretion of androgens from postmenopausal ovary are more, their peripheral levels reduce due to conversion of androgens to estrone in adipose tissue. However, the cumulative effect is a decrease in estrogenic: androgen ratio. This Results in increased facial hair growth and change in voice. As the higher weight patient converts more androgens into estrone, they are less likely to develop symptoms of oestrogen deficiency and osteoporosis. But they are Vulnerable to endometrial hyperplasia and endometrial carcinoma.[1]